Production of Interleukin-1αand a Parathyroid Hormone-Like Factor by a Squamous Cell Carcinoma of the Esophagus (EC-GI) Derived From a Patient With Hypercalcemia*

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Abstract
To determine the pathogenesis of humoral hypercalcemia associated with esophageal carcinoma in a 65-yrold patient, clonal cell lines (EC-GI) were established from the tumor. The EC-GI cells produced bone-resorbing activity which eluted from a Sephadex G-75 column in a broad peak, with an apparent mol wt of 10,000–50,000. In addition to PTH-like factor(s), the EC-GI cells produced a factor with thymocyte proliferation-stimulating activity which had an apparent mol wt of 15,000–20,000. This interleukin-1 (IL-l)-like factor(s) with acidic pi (4.8 and 5.2) exactly coeluted with the bone-resorbing activity upon DEAE-Sepharose ion exchange chromatography. Both bone-resorbing and thymocyte proliferation-stimulating activities were completely inhibited by anti-IL-lα antiserum, but not by anti-IL-1β antiserum. Northern blot hybridization studies revealed that EC-GI cells produced exclusively mRNA for IL-lα. Furthermore, fractions containing IL-1-like activity and PTH-like activity synergistically stimulated bone resorption in vitro, and transplantation of EC-GI cells into nude mice caused hypercalcemia in vivo. These findings suggest that IL-1α and PTH-like factor produced by this squamous cell carcinoma synergistically stimulate bone resorption and are related to humoral hypercalcemia in tumor-bearing nude mice and in the patient.

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